Poor perfusion and disrupted microcirculation of the skin

Poor perfusion of blood to the skin may result from a range of pathological factors such as cardiovascular disease due to arteriosclerosis and heart failure, the effects of oedema and trauma and the occlusion of blood vessels due to pressure. For critically ill patients, the circulatory failure associated with hypovolemia and low cardiac output is associated with redistribution of blood flow caused by increased vasoconstriction, which leads to a decrease in skin perfusion. Therefore, the degree of skin perfusion may reflect the adequacy of global blood flow. The clinical signs of poor skin perfusion include evidence of cold, pale, clammy and mottled skin.

Oedema and lymphoedema
Oedema and lymphoedema may disrupt the microcirculation thereby impairing the skin barrier. Oedema may be caused by heart failure, nephrosis, inflammation, venous hypertension, lymphatic impairment due to cancer and related therapy, filariasis, immobility and congenital and traumatic factors (Ryan, 2008) Chronic oedema is a common problem with at least 100,000 patients affected in the UK alone; it is also poorly identified by health professionals (Moffatt et al., 2003). Chronic oedema is tissue swelling that remains over 3 months, which is not relieved by elevation or diuretics. A useful indicator is a positive Stemmer’s sign – the inability to pinch fold of skin at the base of second toe due to thickening. As a consequence this may impair the skin barrier leading to associated skin changes: these may include the following: dry flaky skin; hyperkeratosis – hard, scaly skin, development of skin creases around the toes and ankles; increased subcutaneous tissue; fibrosis of the tissue and lymphangioma, where there are blister-like bulging of dilated lymphatic vessels papillomatosis, with a cobblestone effect on the skin due to lymphangioma and fibrosis. The skin may be further impaired due to the greater subsequent risk of infection.

Lymphoedema is an accumulation of lymph in the tissues, producing swelling; the legs are most often affected, but arms and genitalia may also be involved. It may be due to a congenital abnormality of the lymphatic vessels, as in Milroy’s disease, congenital lymphoedema of the legs or result from obstruction (Martin and McFerran, 2008).

Lymphoedema for clinical problems other than cancer treatment is much more prevalent than generally perceived, although the resources are mainly cancer service based.

Skin problems seen in lymphoedema include the following: (1) hyperkeratosis (an over proliferation of the keratin layer, (2) folliculitis, (3) fungal infections, (4) ulceration, (5) venous eczema, (6) contact dermatitis, (7) lymphangiectasia (soft fluid-filled projections caused by the dilatation of lymphatic vessels), (8) papillomatosis (firm raised projections of skin due to raised lymphatic vessels and fibrosis), (9) lymphorrhoea (the leakage of lymph from the skin surface) and (10) cellulitis/ erysipelas.

Pressure
An efficient skin barrier is dependent on an adequate perfusion of blood. The primary effect of pressure on the skin is to occlude capillaries and thereby disrupt blood flow and the carriage of nutrients to the tissues. Pressure effects may arise due to immobility, commonly bed rest or spending prolonged periods in a chair. Pressure effects on the skin have been the subject of extensive research.

The European Pressure Ulcer Advisory Panel (EPUAP) website defines a pressure ulcer as an area of localised damage to the skin and underlying tissue caused by pressure or shear and/or a combination of these (EPUAP, 2008). Nixon (2001) outlines the distinction between the aetiology and pathology of pressure ulcers. Autoregulatory systems that affect blood flow during and following pressure effects are highly relevant to pressure ulcer aetiology. These include the raising of capillary pressure to maintain flow, intermittent flow at subcritical pressures and response to repetitive loading and the reactive hyperaemic response following partial or full occlusion. Such occlusion leads to anoxia and a related accumulation of metabolites. Following pressure release, the large and rapid increase in blood flow through the deprived tissues is termed reactive hyperaemia. Key mechanisms include those that are myogenic and metabolic, related to the metabolite release from either anoxic tissues or the lack of oxygen. The degree and duration of the hyperaemic response is related to the duration of occlusion (Walmsley and Wiles, 1990) and factors such as age (with the elderly being very vulnerable), smoking, vascular or related disease (e.g. diabetes) and conditions such as end-stage renal failure and spinal cord injury. Another important factor is the repetitive loading of pressure, which operates via an active vasomotor response mechanism (Bader, 1990).

The different types of pressure ulcer include those related to epidermal or dermal necrosis, deep pressure ulcers with necrosis occurring within the subcutaneous tissues and full thickness wounds of dry black eschar. The key pathological mechanisms include injury caused by abrupt reperfusion of the capillary bed following occlusion of blood flow, damage to the vasculature due to forces such as shear and cell death arising from prolonged direct occlusion of blood vessels (Nixon, 2001).